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  1. AU="Chiaverina, Giulia"
  2. AU="Saunders, Gary I"
  3. AU="Ng, Liqi"
  4. AU="Kato, Takeshi"
  5. AU="Dalstra, Michel"
  6. AU="Ruben, Jurjen"
  7. AU="Peersman, Nele"
  8. AU=Yip Christina Y C AU=Yip Christina Y C
  9. AU=Mehan Vivek K.
  10. AU="Nara, Akina"
  11. AU=Saccente Michael
  12. AU="Wang, Xiulu" AU="Wang, Xiulu"
  13. AU="Milnes, Di"
  14. AU=Almudhi Abdulaziz
  15. AU="Kumowski, Nina"
  16. AU="Dedeke, Iyabode"
  17. AU="Srivastava, Mitul"
  18. AU=Que Jian-Yu
  19. AU="Midulla, Martina"
  20. AU="et al"
  21. AU="Pritchard, Jonathan"
  22. AU="Memeo, Lorenzo"
  23. AU="Taylan, Gokay"
  24. AU="Tijssen, Robert J. W."
  25. AU="Silva, Marcelina Jasmine"
  26. AU="Egbuna, Chukwuebuka"

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  1. Artikel ; Online: Dynamic Interplay between Pericytes and Endothelial Cells during Sprouting Angiogenesis.

    Chiaverina, Giulia / di Blasio, Laura / Monica, Valentina / Accardo, Massimo / Palmiero, Miriam / Peracino, Barbara / Vara-Messler, Marianela / Puliafito, Alberto / Primo, Luca

    Cells

    2019  Band 8, Heft 9

    Abstract: Vascular physiology relies on the concerted dynamics of several cell types, including pericytes, endothelial, and vascular smooth muscle cells. The interactions between such cell types are inherently dynamic and are not easily described with static, ... ...

    Abstract Vascular physiology relies on the concerted dynamics of several cell types, including pericytes, endothelial, and vascular smooth muscle cells. The interactions between such cell types are inherently dynamic and are not easily described with static, fixed, experimental approaches. Pericytes are mural cells that support vascular development, remodeling, and homeostasis, and are involved in a number of pathological situations including cancer. The dynamic interplay between pericytes and endothelial cells is at the basis of vascular physiology and few experimental tools exist to properly describe and study it. Here we employ a previously developed ex vivo murine aortic explant to study the formation of new blood capillary-like structures close to physiological situation. We develop several mouse models to culture, identify, characterize, and follow simultaneously single endothelial cells and pericytes during angiogenesis. We employ microscopy and image analysis to dissect the interactions between cell types and the process of cellular recruitment on the newly forming vessel. We find that pericytes are recruited on the developing sprout by proliferation, migrate independently from endothelial cells, and can proliferate on the growing capillary. Our results help elucidating several relevant mechanisms of interactions between endothelial cells and pericytes.
    Mesh-Begriff(e) Animals ; Aorta/cytology ; Aorta/metabolism ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Mice ; Mice, Transgenic ; Neovascularization, Physiologic ; Pericytes/cytology ; Pericytes/metabolism
    Sprache Englisch
    Erscheinungsdatum 2019-09-19
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells8091109
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: PI3K/mTOR inhibition promotes the regression of experimental vascular malformations driven by PIK3CA-activating mutations.

    di Blasio, Laura / Puliafito, Alberto / Gagliardi, Paolo Armando / Comunanza, Valentina / Somale, Desiana / Chiaverina, Giulia / Bussolino, Federico / Primo, Luca

    Cell death & disease

    2018  Band 9, Heft 2, Seite(n) 45

    Abstract: Somatic activating mutations within the PIK3CA gene have been recently detected in sporadic lymphatic and venous malformations, and in vascular malformations (VM) associated to overgrowth syndromes, such as CLOVES and Klippel-Trenaunay syndrome. Although ...

    Abstract Somatic activating mutations within the PIK3CA gene have been recently detected in sporadic lymphatic and venous malformations, and in vascular malformations (VM) associated to overgrowth syndromes, such as CLOVES and Klippel-Trenaunay syndrome. Although VM are often limited to specific tissue areas and can be well treated, in extended or recurrent lesions novel therapeutic approaches are needed. We generated a mouse model of VM by local expression of PIK3CA-activating mutation in endothelial cells. PIK3CA-driven lesions are characterized by large areas of hemorrhage, hyperplastic vessels, infiltrates of inflammatory cells, and elevated endothelial cell density. Such vascular lesions are ameliorated by administration of dual PI3K/mTOR inhibitor, BEZ235, and mTOR inhibitor, Everolimus. Unexpectedly, the expression of PIK3CA-activating mutations in human endothelial cells results in both increased proliferation rates and senescence. Moreover, active forms of PIK3CA strongly promote the angiogenic sprouting. Treatment with PI3K/mTOR inhibitors restores normal endothelial cell proliferation rate and reduces the amount of senescent cells, whereas treatment with Akt inhibitor is less effective. Our findings reveal that PIK3CA mutations have a key role in the pathogenesis of VM and PIK3CA-driven experimental lesions can be effectively treated by PI3K/mTOR inhibitors.
    Mesh-Begriff(e) Animals ; Cattle ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Embryo, Mammalian ; Endothelial Cells ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Umbilical Cord ; Vascular Malformations/genetics ; Vascular Malformations/metabolism ; Vascular Malformations/pathology
    Chemische Substanzen Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, mouse (EC 2.7.1.1) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CA protein, human (EC 2.7.1.137) ; Pik3ca protein, mouse (EC 2.7.1.137)
    Sprache Englisch
    Erscheinungsdatum 2018-01-19
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-017-0064-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Activation of RSK by phosphomimetic substitution in the activation loop is prevented by structural constraints.

    Somale, Desiana / Di Nardo, Giovanna / di Blasio, Laura / Puliafito, Alberto / Vara-Messler, Marianela / Chiaverina, Giulia / Palmiero, Miriam / Monica, Valentina / Gilardi, Gianfranco / Primo, Luca / Gagliardi, Paolo Armando

    Scientific reports

    2020  Band 10, Heft 1, Seite(n) 591

    Abstract: The activation of the majority of AGC kinases is regulated by two phosphorylation events on two conserved serine/threonine residues located on the activation loop and on the hydrophobic motif, respectively. In AGC kinase family, phosphomimetic ... ...

    Abstract The activation of the majority of AGC kinases is regulated by two phosphorylation events on two conserved serine/threonine residues located on the activation loop and on the hydrophobic motif, respectively. In AGC kinase family, phosphomimetic substitutions with aspartate or glutamate, leading to constitutive activation, have frequently occurred at the hydrophobic motif site. On the contrary, phosphomimetic substitutions in the activation loop are absent across the evolution of AGC kinases. This observation is explained by the failure of aspartate and glutamate to mimic phosphorylatable serine/threonine in this regulatory site. By detailed 3D structural simulations of RSK2 and further biochemical evaluation in cells, we show that the phosphomimetic residue on the activation loop fails to form a critical salt bridge with R114, necessary to reorient the αC-helix and to activate the protein. By a phylogenetic analysis, we point at a possible coevolution of a phosphorylatable activation loop and the presence of a conserved positively charged amino acid on the αC-helix. In sum, our analysis leads to the unfeasibility of phosphomimetic substitution in the activation loop of RSK and, at the same time, highlights the peculiar structural role of activation loop phosphorylation.
    Mesh-Begriff(e) Amino Acid Motifs ; Amino Acid Substitution ; Enzyme Activation ; Evolution, Molecular ; HEK293 Cells ; HeLa Cells ; Humans ; Models, Molecular ; Molecular Dynamics Simulation ; Molecular Mimicry ; Phosphorylation ; Phylogeny ; Protein Structure, Secondary ; Ribosomal Protein S6 Kinases, 90-kDa/chemistry ; Ribosomal Protein S6 Kinases, 90-kDa/genetics ; Ribosomal Protein S6 Kinases, 90-kDa/metabolism
    Chemische Substanzen Ribosomal Protein S6 Kinases, 90-kDa (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2020-01-17
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-56937-3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: MRCKα is activated by caspase cleavage to assemble an apical actin ring for epithelial cell extrusion.

    Gagliardi, Paolo Armando / Somale, Desiana / Puliafito, Alberto / Chiaverina, Giulia / di Blasio, Laura / Oneto, Michele / Bianchini, Paolo / Bussolino, Federico / Primo, Luca

    The Journal of cell biology

    2017  Band 217, Heft 1, Seite(n) 231–249

    Abstract: Extrusion of apoptotic cells from epithelial tissues requires orchestrated morphological rearrangements of the apoptotic cell and its neighbors. However, the connections between the apoptotic cascade and events leading to extrusion are not fully ... ...

    Abstract Extrusion of apoptotic cells from epithelial tissues requires orchestrated morphological rearrangements of the apoptotic cell and its neighbors. However, the connections between the apoptotic cascade and events leading to extrusion are not fully understood. Here, we characterize an apoptotic extrusion apical actin ring (EAAR) that is assembled within the apoptotic cell and drives epithelial extrusion. Caspase-mediated cleavage of myotonic dystrophy kinase-related CDC42-binding kinase-α (MRCKα) triggers a signaling pathway that leads to the assembly of EAAR that pulls actin bundles, resulting in the compaction and removal of the cell body. We provide a detailed portrait of the EAAR including F-actin flow, the contribution of myosin contraction, and actin polymerization at bundles' terminals when the product of MRCKα cleavage is expressed. These results add to our understanding of the mechanisms controlling the process of epithelial extrusion by establishing a causal relationship between the triggering events of apoptosis, the activation of MRCKα, and its subsequent effects on the dynamics of actomyosin cytoskeleton rearrangement.
    Mesh-Begriff(e) Actin Cytoskeleton/metabolism ; Actins/metabolism ; Actomyosin/metabolism ; Animals ; Apoptosis/physiology ; Caco-2 Cells ; Cardiac Myosins/metabolism ; Caspases/metabolism ; Cell Line ; Dogs ; Epithelial Cells/metabolism ; HEK293 Cells ; HeLa Cells ; Humans ; Madin Darby Canine Kidney Cells ; Microtubule-Organizing Center/physiology ; Myosin Light Chains/metabolism ; Myosins/metabolism ; Myotonin-Protein Kinase/metabolism ; Signal Transduction/physiology ; rho-Associated Kinases/metabolism
    Chemische Substanzen Actins ; Myosin Light Chains ; myosin light chain 2 ; Actomyosin (9013-26-7) ; CDC42BPA protein, human (EC 2.7.1.-) ; Myotonin-Protein Kinase (EC 2.7.11.1) ; ROCK1 protein, human (EC 2.7.11.1) ; rho-Associated Kinases (EC 2.7.11.1) ; Caspases (EC 3.4.22.-) ; Cardiac Myosins (EC 3.6.1.-) ; Myosins (EC 3.6.4.1)
    Sprache Englisch
    Erscheinungsdatum 2017-11-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.201703044
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: The AGMA1 polyamidoamine mediates the efficient delivery of siRNA.

    Cavalli, Roberta / Primo, Luca / Sessa, Roberto / Chiaverina, Giulia / di Blasio, Laura / Alongi, Jenny / Manfredi, Amedea / Ranucci, Elisabetta / Ferruti, Paolo

    Journal of drug targeting

    2017  Band 25, Heft 9-10, Seite(n) 891–898

    Abstract: AGMA1, a prevailingly cationic, guanidine-bearing, linear, amphoteric polyamidoamine is an effective siRNA condensing agent. Here two AGMA1 samples of different molecular weight, i.e. AGMA1-5 and AGMA1-10 were evaluated as siRNA condensing agents and ... ...

    Abstract AGMA1, a prevailingly cationic, guanidine-bearing, linear, amphoteric polyamidoamine is an effective siRNA condensing agent. Here two AGMA1 samples of different molecular weight, i.e. AGMA1-5 and AGMA1-10 were evaluated as siRNA condensing agents and transfection promoters. AGMA1-10 formed stable polyplexes with a size lower than 50 nm and positive zeta potential. AGMA1-5 polyplexes were larger, about 100 nm in size. AGMA1-10 polyplexes, but not AGMA1-5 proved to be an effective intracellular siRNA carrier, able to trigger gene silencing in Hela and PC3 cell lines without eliciting cytotoxic effects. AGMA1-10 knocked down AKT-1 expression upon transfection with an AKT-1 specific siRNA. The polyplex entry mechanism was investigated and was mediated by macropinocytosis. In conclusion, AGMA1 has potential as an efficient, non-toxic tool for the intracellular delivery of siRNA and warrants further investigation.
    Sprache Englisch
    Erscheinungsdatum 2017-11
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1187110-6
    ISSN 1029-2330 ; 1061-186X
    ISSN (online) 1029-2330
    ISSN 1061-186X
    DOI 10.1080/1061186X.2017.1363215
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Modeling human tumor angiogenesis in a three-dimensional culture system.

    Seano, Giorgio / Chiaverina, Giulia / Gagliardi, Paolo Armando / di Blasio, Laura / Sessa, Roberto / Bussolino, Federico / Primo, Luca

    Blood

    2013  Band 121, Heft 21, Seite(n) e129–37

    Abstract: The intrinsic complexity of the process of vessel formation limits the efficacy of cellular assays for elucidation of its molecular and pharmacologic mechanisms. We developed an ex vivo three-dimensional (3D) assay of sprouting angiogenesis with arterial ...

    Abstract The intrinsic complexity of the process of vessel formation limits the efficacy of cellular assays for elucidation of its molecular and pharmacologic mechanisms. We developed an ex vivo three-dimensional (3D) assay of sprouting angiogenesis with arterial explants from human umbilical cords. In this assay, human arterial rings were embedded in basement membrane extract gel, leading to a network of capillarylike structures upon vascular endothelial growth factor (VEGF) A stimulation. The angiogenic outgrowth consisted of endothelial cells, which actively internalized acetylated-low-density lipoprotein, surrounded by pericytes. Computer-assisted quantification of this vascular network demonstrated considerable sensitivity of this assay to several angiogenic inhibitors, including kinase inhibitors and monoclonal antibodies. We also performed targeted gene knockdown on this model by directly infecting explanted umbilical arteries with lentiviruses carrying short-hairpin RNA. Downregulation of VEGFR2 resulted in a significant reduction of the sprouting capability, demonstrating the relevance of human vascular explants for functional genomics studies. Furthermore, a modification of this assay led to development of a 3D model of tumor-driven angiogenesis, in which angiogenic outgrowth was sustained by spheroids of prostate cancer cells in absence of exogenous growth factors. The human arterial ring assay bridges the gap between in vitro endothelial cell and animal model, and is a powerful system for identification of genes and drugs that regulate human angiogenesis.
    Mesh-Begriff(e) Angiogenesis Inhibitors/pharmacology ; Animals ; Aorta/cytology ; Cell Culture Techniques/methods ; Cell Line, Tumor ; Female ; Gene Knockdown Techniques ; Humans ; Imaging, Three-Dimensional/methods ; Lentivirus/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/physiopathology ; Prostatic Neoplasms/blood supply ; Prostatic Neoplasms/pathology ; Transduction, Genetic/methods ; Umbilical Arteries/cytology ; Umbilical Arteries/physiology ; Vascular Endothelial Growth Factor Receptor-2/genetics
    Chemische Substanzen Angiogenesis Inhibitors ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2013-03-07
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2012-08-452292
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Endothelial podosome rosettes regulate vascular branching in tumour angiogenesis.

    Seano, Giorgio / Chiaverina, Giulia / Gagliardi, Paolo Armando / di Blasio, Laura / Puliafito, Alberto / Bouvard, Claire / Sessa, Roberto / Tarone, Guido / Sorokin, Lydia / Helley, Dominique / Jain, Rakesh K / Serini, Guido / Bussolino, Federico / Primo, Luca

    Nature cell biology

    2014  Band 16, Heft 10, Seite(n) 931–41, 1–8

    Abstract: The mechanism by which angiogenic endothelial cells break the physical barrier of the vascular basement membrane and consequently sprout to form new vessels in mature tissues is unclear. Here, we show that the angiogenic endothelium is characterized by ... ...

    Abstract The mechanism by which angiogenic endothelial cells break the physical barrier of the vascular basement membrane and consequently sprout to form new vessels in mature tissues is unclear. Here, we show that the angiogenic endothelium is characterized by the presence of functional podosome rosettes. These extracellular-matrix-degrading and adhesive structures are precursors of de novo branching points and represent a key feature in the formation of new blood vessels. VEGF-A stimulation induces the formation of endothelial podosome rosettes by upregulating integrin α6β1. In contrast, the binding of α6β1 integrin to the laminin of the vascular basement membrane impairs the formation of podosome rosettes by restricting α6β1 integrin to focal adhesions and hampering its translocation to podosomes. Using an ex vivo sprouting angiogenesis assay, transgenic and knockout mouse models and human tumour sample analysis, we provide evidence that endothelial podosome rosettes control blood vessel branching and are critical regulators of pathological angiogenesis.
    Mesh-Begriff(e) Animals ; Basement Membrane/metabolism ; Cell Line, Tumor ; Cell Membrane Structures/drug effects ; Cell Membrane Structures/metabolism ; Cell Membrane Structures/physiology ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelial Cells/physiology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; HEK293 Cells ; HeLa Cells ; Humans ; Integrin alpha6beta1/genetics ; Integrin alpha6beta1/metabolism ; Laminin/metabolism ; Lung Neoplasms/blood supply ; Lung Neoplasms/metabolism ; Lung Neoplasms/physiopathology ; Male ; Matrix Metalloproteinase 14/metabolism ; Melanoma, Experimental/blood supply ; Melanoma, Experimental/metabolism ; Melanoma, Experimental/physiopathology ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Confocal ; Microscopy, Fluorescence ; Neoplasms/blood supply ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/physiopathology ; RNA Interference ; Tetradecanoylphorbol Acetate/pharmacology ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor A/pharmacology
    Chemische Substanzen Integrin alpha6beta1 ; Laminin ; Vascular Endothelial Growth Factor A ; Green Fluorescent Proteins (147336-22-9) ; Matrix Metalloproteinase 14 (EC 3.4.24.80) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
    Sprache Englisch
    Erscheinungsdatum 2014-09-14
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/ncb3036
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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